The fundamental event of effective and persistent humeral immunity is the germinal center (GC) reaction. This reaction arises from the interaction of antigen-specific B- and T-lymphocytes within a reticulum formed by the processes of follicular dendritic cells (FDC). Under physiologic conditions, the GC response is necessary for V(D)J hypermutation and the selection of B-cells that secrete high affinity antibody, establishment of long-lived plasmacyte populations that maintain serum antibody levels, and generation of the memory B-cell compartment. Although the cellular components of the GC reaction have been identified generally, relatively little is known regarding the exact nature of the T- and B lymphocytes that enter the FDC network to form the nascent GC. Almost nothing is understood about the interactions that mediate the activation of hypermutation nor the differentiation that that leads to the long-lived plasmacyte and memory cell populations. We have identified a novel T-cell population that uniquely supports the characteristic cellular reactions of T-cell dependent humeral immunity, the GC reaction, V(D)J hypermutation, and B-cell memory. We shall determine at what point expression of the BCL-6 transcription represser becomes crucial for lymphocyte migration into the germinal center and study how T-cells and inflammatory signals influence the expansion/activation of FDC networks. We shall characterize this novel T-cell population and define the molecular signals that initiate and or support the GC reaction, hypermutation, and the generation of B-cell memory.